of ME and CFS patients. How such patients are defined appears to make
a significant difference.
Autoimmune Dis. 2012;2012:189096. Epub 2012 Jan 24.
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D
Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis.
Pender MP.
School of Medicine, The University of Queensland, Brisbane, QLD 4072, Austr=
alia.
Abstract
CD8+ T-cell deficiency is a feature of many chronic autoimmune
diseases, including multiple sclerosis, rheumatoid arthritis, systemic
lupus erythematosus, Sj=F6gren's syndrome, systemic sclerosis,
dermatomyositis, primary biliary cirrhosis, primary sclerosing
cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo,
bullous pemphigoid, alopecia areata, idiopathic dilated
cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's
thyroiditis, myasthenia gravis, IgA nephropathy, membranous
nephropathy, and pernicious anaemia.
It also occurs in healthy blood relatives of patients with autoimmune
diseases, suggesting it is genetically determined. Here it is proposed
that this CD8+ T-cell deficiency underlies the development of chronic
autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr
virus (EBV) infection, with the result that EBV-infected autoreactive
B cells accumulate in the target organ where they produce pathogenic
autoantibodies and provide costimulatory survival signals to
autoreactive T cells which would otherwise die in the target organ by
activation-induced apoptosis.
Autoimmunity is postulated to evolve in the following steps: (1) CD8+
T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+
T-cell control of EBV, (4) increased EBV load and increased anti-EBV
antibodies, (5) EBV infection in the target organ, (6) clonal
expansion of EBV-infected autoreactive B cells in the target organ,
(7) infiltration of autoreactive T cells into the target organ, and
(8) development of ectopic lymphoid follicles in the target organ.
It is also proposed that deprivation of sunlight and vitamin D at
higher latitudes facilitates the development of autoimmune diseases by
aggravating the CD8+ T-cell deficiency and thereby further impairing
control of EBV. The hypothesis makes predictions which can be tested,
including the prevention and successful treatment of chronic
autoimmune diseases by controlling EBV infection.
The full study can be found here:
http://www.hindawi.com/journals/ad/2012/189096/
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